Hemagglutinating Encephalomyelitis (Vomiting and Wasting Disease)

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A disease seen in pigs less than four weeks old, characterized by signs that include vomiting, wasting and, perhaps, neurologic signs.


Hemagglutinating encephalomyelitis (HE) occurs only in swine. The disease occurs in most major swine-raising countries but tends to be quite sporadic. Infection is clinically silent except in piglets less than four weeks old. In these, the disease occurs as an acute outbreak affecting most piglets in litters of nonimmune dams.

Historical information

In 1959 an encephalomyelitis of suckling pigs was reported in Ontario, Canada. In 1962, other investigators reported a hemagglutinating virus producing encephalomyelitis in baby pigs. In 1969, vomiting and wasting disease, similar in many respects to the encephalomyelitis reported in Canada, was reported in England. Viruses from the outbreaks later were proven to be similar or identical.

Much of the research on HE infection in swine was completed in the 1970s and 1980s. Epidemiologic studies have shown the virus to be widespread in the US. However, clinical outbreaks seldom occur and the disease is of modest economic importance.


Two overlapping syndromes are caused by a single hemagglutinating coronavirus. The virus can be grown in several porcine cell culture systems and hemagglutinates erythrocytes from several kinds of animals. Only one serotype of the virus is recognized. Differences in strain virulence, along with differences in susceptibility, are responsible for the two syndromes. The virus is moderately resistant to destructive environmental factors.


Only pigs are susceptible. Transmission of virus is presumably through actively infected or carrier swine. Exposure is probably through infectious nasal secretions or aerosol. Most large breeding herds in major swine-raising countries are endemically infected. In most swine herds, immune sows provide colostral antibody that protects their piglets for 4-18 weeks. Passive immunity in the growing pigs is replaced by active immunity as a consequence of exposure to virus in the environment followed by subclinical infection. Clinically apparent disease develops only when young piglets from nonimmune sows are exposed.


Transmitted virus replicates in the nasal epithelial mucosa, tonsils, lungs and small intestine and spreads via the peripheral nervous system to the central nervous system (CNS). Viremia is probably of little significance in spread. In the CNS, virus localizes first in nuclei in the medulla oblongata but later progresses to the brain stem, spinal cord and sometimes to the cerebrum and cerebellum. The virus produces lesions in a variety of nuclei, ganglia and plexi (trigeminal ganglion, vagal sensory nuclei, some brain stem nuclei, intramural plexi of the stomach). Clinical signs vary, depending upon which nuclei are affected by the virus. Death occurs whenever a vital nucleus ceases to function.

Clinical signs

Vomiting and wasting syndrome: Sneezing and coughing may occur at onset. Within a few days, vomiting of milk and retching are prominent signs. The young pigs dehydrate rapidly and often grind their teeth. When water is supplied, piglets mouth it but drink little, presumably because of pharyngeal paralysis. After a few days they exhibit dyspnea, cyanosis, coma and die.

Pigs in older litters survive longer but continue to vomit occasionally. The anterior abdomen of some of them may become distended, presumably from impaired emptying and accumulation of gas. Most affected piglets waste away over a few weeks and die. The few that survive remain unthrifty. Morbidity and mortality in both syndromes approaches 100% in affected litters.

Encephalomyelitis syndrome: Initial signs are similar to those in the above syndrome. Vomiting and retching occur less often and lead to less dehydration. In one to three days, any of a variety of signs of encephalomyelitis appear. These may include: stilted gait, muscle tremors, nystagmus, blindness, opisthotonus, convulsions, and progressive paresis leading to recumbency with paddling of the legs. Occasional pigs walk backwards and assume a dog-sitting position. Affected pigs soon weaken, pass into coma and die. In some litters of older pigs, there may be only transient posterior paresis followed by recovery.


Lesions are similar in the two syndromes. Chronically infected pigs have cachexia and there may be distension of the anterior abdomen by excessive gas in the stomach.

Microscopic lesions include a nonsuppurative encephalitis affecting the gray matter of the medulla and brain stem. The frequency of lesions at specific sites may vary in the two syndromes. There is inflammation of the trigeminal, paravertebral and autonomic ganglia. Also, ganglia in the stomach wall, mostly in the pyloric area, may show degeneration.


The history, signs, and age group affected may suggest the diagnosis. Microscopic lesions, also, are helpful in diagnosis. However, for definitive diagnosis the virus should be isolated and identified. Isolation can best be made from the brain stem of piglets showing signs for less than two days. Paired early and late serum samples sometimes can be used to show a rise in antibody titer against the infection. The first blood samples should be taken early in the course of the disease since antibody levels rise quickly. There does not appear to be serologic cross-reaction with other porcine coronaviruses (transmissible gastroenteritis [TGE], porcine respiratory coronavirus [PRCV]).


Hyperimmune serum or serum from swine of an immune herd can be given for prevention during the early stages of an outbreak. However, outbreaks run their course so rapidly (two to three weeks), the time necessary for diagnosis and obtaining serum makes this impractical.

Once the virus is introduced, it persists in the herd. Most breeding stock has been exposed, has developed an active immunity and provides adequate passive immunity for their piglets.

There is no effective treatment.